Notes from Medicine Teaching

Renal
AKI and CKD
 Jobs of the kidney
o Waste
o Electrolyte balance
o Acid-base balance
o Fluid balance
o EPO
 70yo male patient, T2DM, ex-smoker, dehydration, AKI —> treatment with oxygen, IVI, IV
antibiotics, bloods, MSC, urine dip, examination, ABG (lactate), cultures, ECG, CXR, stool
culture
 Dehydration v overload - peripheral/pulmonary oedema, JVP, SOB, sacral oedema, mucous
membranes, skin turgor, lying/standing BP
 Albumin - low (in teens), then if no oedema they are dry
 Normal saline for dehydration —> 4 hourly, fluid bolus 500ml NS over 20 minutes, check for
response within 1 hour, can repeat process
 Uraemia - not passing urine - insensible losses = 500ml (UO + losses = maintenance)
 Dialysis acutely if:-
o Hyperkalaemia (refractory)
o Uraemic encephalopathy
o Acidosis
o Uraemic pericarditis - ECG (saddle, sinus tachycardia, widespread concave ST
elevation and PR depression in limb leads, and V2-V6), pain, rub
o Fluid overload
 Uraemia
o Asterixis
o Pericarditis
o Confusion
 Haemodialysis V Filtration (slower)
 Acute tubular necrosis - can take up to 2 weeks to re-establish
o Biopsy after 1/52
 Renal Screen
o ANCA antibodies - MPO (Churg-Strauss v microscopic) /MP3 (granulomatosis with
polyangiitis)
o Immunoglobulins with electrophoresis - myeloma, high calcium, light chains,
amyloid, light chain nephropathy (urine and blood), Benz Jones protein (multiple
myeloma)
o Anti-IgBM = against glomerular BM = renal failure and pulmonary haemorrhage
good pasture
o Anti-nuclear antibody - SLE, complement C3 and C4 low
o Post-strep nephritis shows ASOT - anti-streptolysin - antibody against toxic enzyme
from group A strep
 NB IgA often chronic not acute
 Goodpasture syndrome - renal-pulmonary syndrome
 CKD
o Stage 1
o Stage 2
o Stage 3
  Stage 3a - eGFR 45-60
 Stage 3b - 35-45
o Stage 4 - 15-30
o Stage 5 - Under 15 or renal replacement therapy
 IN CKD need to check bloods including anaemia, electrolytes, HCO3, calcium, phosphate,
secondary hyperparathyroidism (check PTH), potassium (allow up to 6), albumin
o If tertiary hyperparathyroidism then cinacalet treatment to suppress PTH
o ACEI slows progression of CKD if DM +/- proteinuria
o Check BP - aim for 130/80
o Blood sugar control
o Stop smoking
 Treatment
o BP
o Anaemia - check B12, any bleeds, folate, iron, ferritin, etc —> haematemesis, IV iron,
EPO (aim for 10-12), if asymptomatic OR under 10
o Activated vitamin D
o Dietician involvement
o Oral NaHCO2 tablets (sodium, increase BP, fluid retention)
 CKD progression - think ahead, rate of decline in function - dialysis, transplant, conservative
care
o Fistula placement once eGFR under 20
 Dialysis (SE include metallic taste, pruritis, loss of appetite, weight loss)
o Haemodialysis (home)
o Peritoneal dialysis (home or PD tube)
Coca-Cola Urine
 Haemolysis - low platelet, onto skin conjunctiva, factor - into muscles, joints, renal pelvis,
ICH
 Rhabdomyolysis - damage to BM (glomerulonephritis, ghost RBC - RBC casts)
o renal stones, trauma, catheter, kidney tumour, pyelonephritis, bladder cancer (TCC)
 +ve blood on RBC on MSU (+ve or -ve), RBC or myoglobin or Hb
 Causes
o Haemolysis
o Glomerulonephritis
o Damage to urothelial
 Extravascular
o Spleen - immune function (LN)
o Breakdown RBC
o No spleen - antimalarials, antibiotics
 Intravascular (should NOT happen)
o Cutting - MAHA - HUS/TTP (E.coli 0157, toxin damages endothelium), malignant
HTN, AS, bilirubin high, Eclampsia (HELLP), DIC - bleed to death, run out of clotting
factors (high INR, high APTTR, low platelet, low Hb, high D-dimer) - malaria
o Smashing - metallic heart valve, with vegetation, march/bongo haematuria
o Punching
o Another - malaria
Transplant
 Azathioprine - inhibit production of purines, decrease proliferation B/T cells, antimetabolite
 Ciclosporin - anti-proliferative
 Transplant - 10-15 years life extended, and increase QoL with better food/diet, fertility
restored, high energy levels, low overall cost
  CKD increases CVD risk —> calcification of blood vessels
 Risks of treatment include symptomatic risk, rejection, increase infection risk, SE of
immunosuppression, increased risk of malignancy (lymphoma and SCC due to decrease
immune surveillance
 Immunology in transplant
o Blood type (ABO)
o HLA - histocompatibility locus antigen - chromosome 6
 Class I (A/B/C) - CD8 + T cell recognition
 Class II - DP/DQ/DR = CD4 and T cell recognition
 DR = most antigenic
 Class III
 IL2 — lymphocytic proliferation
 Ciclosporin - blocks calcineurin, stop proliferation, tacrolimus
 Balance immunosuppression - balancing infection/malignancy with rejection
 Treatment
o Induction - steroids, (anti-inflamatory and immunosuppression), anti-CD25
(basiliximab), ATG, campath/atemtuzumab (anti-CD52) for lymphocytic depletion
o Maintenance - anti-metabolite (MMF + azathioprine, CI pregnancy and SE GI),
steroids, anti-proliferative (calcineurin inhibitor such as tacrolimus, ciclosporin)
o Adjustments - steroid withdrawal, monotherapy, switch to mTOR inhibitors
 Calcineurin inhibitor - HTN/nephrotoxic/DM/dyslipidaemia, narrow therapeutic index,
NODAT (diabetes post transplant), cytochrome P450, tacrolimus
 Donors
o Live donation
o DBD, DCD
Arrhythmia
 Tachycardia V bradycardia
o Patient well, regular/irregular, where/why in hospital, observations - BP, try fluids
o Narrow - bundle of his, SVT, SAN, AVN, atria
o High HR, narrow QRS, P waves
o Patient unwell - no response to fluid
 Tachycardia, hypotension - electricity DC cardioversion/chemical cardioversion
 Tachycardia - narrow or broad
o Narrow P waves = sinus tachycardia/atrial tachycardia
o Narrow no P waves = AF (irregular), SVT (atrial tachycardia, atrioventricular nodal re-
entry), AVRT/AVNRT, flutter (regular)
 B-blockers - +/- digoxin, flecainide (need ECHO), verapamil/dilitizaem, amiodarone in elderly
 Adenosine, low AVN, cut circuit, will feel tight, unwell, 6mg
PE/DVT
 Risk factors - malignancy, surgery (legs/hips/gynae), previous PE/DVT, pregnancy, immobility
(long haul flights), thrombophilias
 Present with SOB, haemoptysis, swollen/calf tenderness, chest pain, pleuritic pain, acute,
sudden cariogenic shock
 ABCDE - hypoxia, SpO2, tachycardia, tachypnoea, BP normal or low
o Correct oxygen to 94-98%
o WELLS score = subjective, probability
o ECG - tachycardia, RV strain (T wave inversion, V1-V2 inferior leads, R axis deviation,
RBBB
o Bloods - FBC (anaemia, WCC, platelets), U&E (contrast used, baseline), clotting -
platelets, heparin (INR)
 o Blood gas - normal/low CO2 and low O2
 NB signs of shock usually tachycardia, hypotension (except in neurogenic low HR and high
BP)
 ABG
o Normal lungs but small PE - pCO2 low due to hyperventilation, O2 will be normal or
low (NB normal is low!)
o Massive PE - low pH, low pCO2, low oxygen and low BE
o NB if low pO2 then issue with lungs or cardiac shunt (from R to L)
o Metabolic acidosis - DKA, septicaemia, poison, pneumonia with sepsis, PE
 Tachypnoea - drop in CO2, O2 up to 16/17 normally
 T1RF less than 8, fall of dissociation curve
 Hypoxia - no air in, no exchange, lung V/Q mismatch, vasculature, alveoli, interstitium, no air
out, blood to LV (blocked by PE)
 Shunt = einsenmengers, tetralogy of fallot, transposition of great arteries
 15min/L, normal O2 but Not with oxygen
 CXR - pneumothorax, exclude structural cause
o Wedge shaped infarct, increased opacification in hillier region, linear atelectasis
(base), absence of flow (bullae)
o CTPA - if lug disease/abnormal CXR, can miss a small PE, clot, pick up another cause
o V/Q scan - 100% good to say no, assumes normal lungs, can see small defect
 Treatment - anti-coagulate, NOAC (apixaban), 3/12 if RF gone
 Thrombolyse if shock or hypotension
 Provoked V unprovoked
o 3 months anticoagulation
o Unprovoked then look for malignancy (under 40 then do nothing but if over then CT
chest abdo pelvis
o Most commonly breast/testicular and haematological
o Anticoagulate for life if 2 events
o NOAC (all else) v warfarin (if no renal function, below 15 GFR) v LMWH (pregnancy
or cancer)
ACS
 cardiac positive marker
 angina — unstable angina — MI (STEMI or NSTEMI)
 ABCDE (high RR, low Oxygen saturations, high HR, signs of shock)
 ECG - signs of ischemia (ST elevation/depression, T wave inversion, Q waves if full thickness)
 Treatment
o Oxygen - aim for 94-98%, via non-rebreathe/venturi mask
o GTN - vasodilation, give at a tilt not on standing as can cause vasovagal syncope
o Aspiring - dual anti-platelet therapy (aspirin, clopidogrel)
o IV access for morphine - anxiety, pain
 Cardia enzymes
 Heart failure - check for peripheral/pulmonary oedema
 Consider diuretics, statin (80mg atorvastatin)
 Rate control - B-blocker, bisoprolol (aim for rate 50-60)
 Bloods
o ABG - lactate
o Troponin
o FBC - anaemia, Hb, MCV, platelets (anti-platelet therapy 1 year if stent), clotting
o U&E - correct electrolyte imblances (cause arrhythmia), PCA (nephrotoxic drugs),
ACEI (ramipril will drop creating by 10-15% as normal)
  Post-MI
o Conservative - cardiac rehab, healthy BMI, stops making
o Medical - SE (increase/decrease doses, need good compliance) —> GTN
spray/tablet, aspiring, statin, B-blocker, anti-hypertensive (ACEI/CCB)
o Surgical - none
o Consider return to work procedures, DVLA
Upper GI Bleed
 Oesophaegeal cancer - carcinoma, smoking, alcohol, dysphagia (progressive), hiccups, pain,
upper Gi bleed, weight loss, decreasing appetite, 20% 5 year survival
 Gastric cancer - poor survival, indigestion, B12 deficiency
 Varices - portal HTN, alcohol, cirrhosis, bleeding, severe haematemesis, ABCDE (shock, low
BP, cold, sweaty), cross match blood and give blood within 30 minutes, give NaCl or O-ve,
with IV PPI (omeprazole), terlipressin decreases portal pressure, band varices, oxygen,
tranexamic acid, antibiotics
o 4444 = serious haemorrhage protocol
o Observations every 15 minutes
o Ring endoscopy and duty anaesthetist
 Gastritis/ulcer - commonest cause of UGI bleed, NSAIDs, alcohol, steroids, H pylori, food
poisoning, vomiting, indigestion, blood, pain when hungry
o Triple therapy - 2 antibiotics with PPI
o Breathe test/blood/gastric
o 80% ulcers with H. pylori
o PPI - rebound acidity, H2 blocker ranitidine
 Mallory-Weiss tear - recurrent vomiting, PPI
 NB causes of cirrhosis – alcohol, viral hepatitis (B and C), NAFLD, autoimmune diseases,
haemochromotosis, Wilson’s disease
Confusion
 David Is A Sex God Always Putting Most Men Safely Down In Their Correct Place
 definition, incidence, age, sex, geographical, aetiology, pathophysiology, macro/micro
histology, signs/symptoms, diagnoses, investigation, treatment, complications, prognosis
 Altered mental state, common, in the elderly, both sexes
o Causes include delirium (emergency and reversible), depression and dementia
o Symptoms include anything out of the ordinary, change in behaviour, attitude
o Ix include bloods, CXR/AXR, scans (CT brain), cognitive function tests, blood sugar
 Delirium - acute onset, fluctuating curse, consciousness disturbance, change in cognition,
function or perception, ICD10 - diagnostic criteria —> common, important, neurotransmitter
disturbance (acetylcholine decrease and dopamine increase)
o Occurs in elderly, frail, dementia, those with less reserve, can happen to anyone,
visual impairment, alcohol excess, renal impairment, polypharmacy, infection,
dehydration
o Most common cause is DRUGS
o DELIRIUM - drugs, dehydration, electrolyte imbalance, level of pain,
infarct/inflammation/infection, respiratory failure, impacted faeces (constipation),
urinary retention, metabolic disorder (hypoglycaemia, renal/liver/adrenal failure)
 Hyperactive v hypoactive v mixed picture - hypoactive more common and less likely to be
picked up
o Flocculation – playing with sheets
 CAM/4At assessment
 AMTS out of 10
 AMT4 - place, age, DOB and year
  CAM
o A - acute and fluctuating
o I - inattention/impairment of attention
o D - disorganised thinking
o A - altered level of consciousness
 Treat the cause - keep looking for causes, especially in drug history, optimise care,
communication for patient and family
 Consider DOLS/MCA
 Drugs Ach – acetylcholine, pilocarpine, muscarine
 Anti-Ach – neostigmine, edrophonium, rivastigmine, donepezil,
 H/W —> managing delirium OOH, AEME
o Haloperidol 0.5-1mg – start low, go slow, CI parkinsons
Nutrition
 NORMAL LIMITS
o 30ml/kg/day of fluid
o 1g/kg/day of protein
o 30kcals/kg/day
 Undernutrition – alcohol, elderly, illness (chronic), lifestyle
 MUST – chronic illness, BMI, unplanned weight loss
 Micronutrients – vitamins and minerals V macronutrients – gross calories
o May not have weight loss, test magnesium, phosphate, vitamin D, B12
o Wernicke-korsakoff
 Oral nutrition
 Enteric nutrition – common in stroke, NG or NJ tube (stomach motility/paresis), not used in
bowel obstruction, PEG (after 1 month)
 Panenteric nutrition – into vein, no functional GI tract, via PICC line (infection risk high), used
in crohn’s and ischaemic bowel (short bowel, not enough small bowel)
 Refeeding syndrome – low magnesium, potassium and phosphate, decreases on feeding,
LFTs deranged, replace micronutrients and then macronutrients in first 24-48 hours, start on
10kcals/kg/day (can occur if no eating for 1 week)
 Anorexia and bulimia – control, body image, disordered body image, correct physiological
deficiency THEN psychological therapy
 Obesity = over nutrition, metabolic syndrome
o Low activity levels, do not stick to BMR, we seek out more food than we need,
mismatch of in v out
o Orilistat – prevent fat absorption
o Endoscopic procedures are often unsuccessful
o Surgery including gastric band, sleeve, by-pass, currently high motivation - consider
if BMI over 40 and diabetic
Lung Cancer
 RF include smoking, asbestos, heavy metal exposure, lung fibrosis
 Asbestos
o PLEURA – diffuse pleural thickening or pleural plaques, pleural effusions,
mesothelioma
o LUNGS – interstitial lung disease/scarring (asbestosis), lymphangitis (SOB)
 Small cell – rapid killer, treatment in a few weeks/months, treat with chemotherapy
 Non-small cell – squamous/adenocarcinoma, slower growth, adenocarcinoma (smoker or
non-smoker)
 RED FLAGS = haemoptysis, hoarse voice, chest pain, metastasis, SOB, cough, weight loss,
night sweats, SIADH, hypercalcemia (secondary to cancer)
 o Haemoptysis common causes include cancer, infection, PE, TB
 Myopathy of myasthenia – Lambert Eaton (autoimmune disease of neuromuscular junction,
nerve to muscle signal stopped with weakness, dry mouth)
o Hyperreflexia
o Encephalitis
 Apical tumour = Pancoast
o Horners – miosis (constricted pupil), ptosis, anhidrosis, enophthalmos (sinking of
eyeball)
o Hoarseness
 Hypercalcaemia (cancer, sarcoidosis, hyperparathyroidism) – dehydration, treat cause,
bisphosphonates IV
 Bullae
 Investigations – PET (glucose, highly active, light up, contrast), CT, biopsy, TMN staging
 Treatment
o Fitness for surgery
o Radical radiotherapy
o Chemotherapy
o Palliation
 Complications
o Spinal cord compression – incontinence, weakness, sensory, UMN (dexamethasone,
urgent MRI)
o Lymphangitis – treat cause, steroids
 Carcinoid pulmonary tumour – slow growing, benign, flushing, diarrhea
 SIADH – syndrome of inappropriate ADH, hyponatremia in blood, ow serum osmolality, high
urine osmolality, urine sodium concentrated, ADH causes diuresis
o Treat cause, fluid restrict, give tetracycline or ADH antagonists
o Opposite = diabetes insipidus
 Cancer SVC obstruction – treatment ASAP by cause
Acute Monoarthritis
 History – stiffness, locking, give way, rash, ulcers, eyes, infections (GI/GU), systemic, morning
= inflammatory, evening = mechanical, loss of function
o Arthralgia – pain
o Arthritis – with swelling
 Ankylosing spondylitis, PA, reactive arthritis, (gonorrhea in joint)
 PMH – immunocompromised, source of infection (IVDU, injection in joint), pre-existing,
damaged joint, autoimmune condition
 Drugs – diuretics, steroids
 Social – alcohol, diet
 ALWAYS RULE OUT SEPTIC ARTHRITIS
 Sero-ve = reactive arthritis or PA
 Bursitis/cellulitis have normal range of movement
 Viral arthritis = aches everywhere
 AVN/lyme disease
 Investigation – aspiration (4 hours), gram stain, MCNS, crystals, cell count, bloods, x-ray,
blood culture, septic screen (TB), MRI for osteomyelitis
o DON’T DO ASPIRATION IF PROSTHETIC JOINT
o Septic arthritis – 22% polyarticular, IVAbx 2/52, oral 4/52
 Sepsis 6
 Urate crystals -ve bifringement, needle shapes
 Calcium pyrophosphate +ve bifringement, rhomboid shape
Monoarthropathy
 1 joint, inflammation, loss of function, pain, swelling, redness
 CONSIDER
o Gout – overnight, pain, 7-10 days
o Trauma
o Pseudogout
o OA
o Septic arthritis
o Haemoarthritis - warfarin
o Inflammatory – PA/RA
 Investigations/history – onset, time, trauma, diet, duration, change, recurrence, family
history, fever, temperature, unwell generally, IBD, look, feel, move of joint,
o Examine joint above and below, full systemic, rashes, neurovascular assessment
 Reactive arthritis (can’t see, can’t pee, can’t climb a tree) – conjunctivitis, urethritis, arthritis
 Investigations
o X-Ray
o Aspiration of joint
o Bloods – infection, inflammation, uric acid levels, autoimmune (ANA), rheumatoid
factor, anti-CCP
o Give pain killers, treat antibiotics, wash out, orthopaedics, lavage, colchine,
allopurinol, NSAIDs, joint replacement, steroid injections, weight loss, physiotherapy
 Erosions
 Causes of gout – diuretics, alcohol, poor diet, sudden onset – urate level for management of
future attacks
 X-Ray signs
o OA- LOSS – loss of joint space, osteophytes, subcholdral cysts and sclerosis
o RA – loss of joint space, peri-articular osteopenia, justa-artcicular erosions, soft
tissue swelling
o Psoaritic arthritis – central erosions (pencil in cup appearance)
o Gout – punched out lesions in bone – peri-articular tophi
o Pseudogout - chondrocalcinosis
Red Flag Headaches
 Concerning symptoms
o Sudden onset headache (SAH)
o Focal neurological deficit, acute confusion, personality change, new onset recurrent
headaches over 1 month (space occupying lesion/viral encephalitis)
o Head trauma (subdural hemorrhage)
o Fever, neck stiffness, rash, menigism, photophobia (meningitis)
o Females on pill/peri-natal period (venous sinus thrombosis)
o Overweight young person (idiopathic intracranial hemorrhage)
o Daily knife like pain involving an eye (often soon after they fall asleep) +/- autonomic
symptoms (cluster headache)
o Visual disturbance + eye pain (acute glaucoma)
o Worsening by moving/straining/coughing/worse in the morning/disturbed sleep –
organic headache
 Raised ICP – morning headache, nausea/vomiting, LOC, papilloedema
 Acute angle closure pressure glaucoma – red eye, halos
 Migraines – triptans, analgesia, 4-72 hours, propranolol, aura, unilateral, photophobia
 Tension – band around had, response to analgesia, 90%
 Cervical – amytriptylline
  SAH – thunderclap
 Subdural – CT, burr hole, trauma
 Encephalitis – usually vial, often herpetic confusion with headache, MRI/LP with PCR
 Giant cell arteritis – scalp tenderness, jaw claudication, sickness
 Cluster – sharp, very painful, nose dribbling, watery eyes
 Drug induced headache – 15 days/month for 3 months
 Venus sinus thrombosis – pregnant, post-natal (6 weeks), quick onset, MR venogram, LP,
increased ICP around 30, anticoagulation for 6/12 on apixaban
 Idiopathic intracranial HTN – headache, papilloedema, raised ICP (around 40-50), drain 20ml,
acetazolamide, SHUNT, gastric bypass
 Tumours – high dose dexamethasone, radiotherapy
 Suspected SAH – CT brain within 6 hours, LP performed more than 12 hours after onset,
send 4 samples (1 and 3 for cell counts microscopy and culture, 2 for biochemistry and 4 for
chromatography)
 Suspected SoL – CT brain, within 24 hours if signs of raised ICP
 Suspected bacterial meningitis – IV ceftriaxone 2g, urgent senior help, 200mg IV
hydrocortisone, send routine bloods, blood cultures, urgent CT brain scan, unless sings of
elevated ICP also LP with MC&S, glucose, protein +/- viral PCR
 Suspected subdural hemorrhage – CT brain
 Suspected venous sinus thrombosis – LP then MR venogram
 Suspected idiopathic intracranial hypertension, CT brain scan, LP for opening pressure, CSF
to run until under 20
 Suspected acute glaucoma
 Suspected viral encephalitis – start IV acyclovir, urgent MR brain scan, hourly neuro
observations
 Raised ICP
Insulins
 RAPIDS – Humalog, apidra, novorapid, FiASP
o Onset 5-15 minutes, peaks 30-90 minutes, duration 3-5 hours
 SHORT – actrapid, Humulin S
o Onset 30 minutes, peak 2-4 hours, duration 6-8 hours
 INTERMEDIATE – Humulin I, insulatard
o Onset 2-4 hours, peak 4-8 hours, duration 14-16 hours
 LONG – Levemir, Lantus, abasaglad, toujeo, degludec
o Onset 0-2 hours, peak (none), duration 18-24 hours
Cellulitis
 Most common bacterial cause is strep pyogenes (group A), staph aureus is secondary in
patients with injury/ulcers, skin and subcutaneous
 RF alcohol, break in skin, drugs, obesity, immunosuppression, lymphoedema/oedema
 Investigations – blood (FBC, U&E’s, CRP, LFT’s, glucose, blood cultures +/- lactate), swab,
mark area for erythema
o Repeat CRP and WBC on day 2 and 4 for treatment response
o X-ray if suspect osteomyelitis
o Add CK if suspect rhabdomyolysis
o Rigors – uncontrolled shivering, bacteraemia
o Doppler if co-existing DVT
 Management – 1g flucloxacillin PO QDS (clindamycin 300mg QDS If allergic) + ANALGESIA
o If signs of sepsis then IV flucloxacillin 1g QDS (or 1.5g TDS, cefuroxime)
o If MRSA +ve or recent stay then IV vancomycin
 NB aim to switch to PO after 24 hours, monitor response, treat underlying cause also
 o If recurrent then consider prophylactic penicillin V 250mg BV for 6/12
 NB inflammation takes weeks to settle but If systemically well and no pain then no more Abx
 Lymphangitis – red streak in lymph
 CONDITIONS
 Peri-orbital cellulitis – threatens vision, spreads behind the eye can cause meningitis or
venous sinus thrombosis, antibiotics, management with max/fax and ophthalmology
 Necrotizing fasciitis – infection of deeper tissues, cellulitis, progresses to rapid destruction of
muscle facia and overlying subcutaneous fat, very painful, purple, raw, blisteringmay display
crepitus, urgent orthopaedic review, IV tazocin or high dose clindamycin (600-900mg TDS)
(may also add in vancomycin, flucloxacillin)
o ICU review
o Debridement, amputation – orthopaedic review
 Fournier’s gangrene – necrotizing infection of perineum, begins abruptly with severe pain,
spreads rapidly to anterior abdominal wall, gluteal muscles and scrotum and penis – as
above but involve urology
 Infected diabetic foot ulcers can lead to gangrene, joint destruction, commence IV tazocin
and vancomycin, urgent vascular surgical review, start sliding scale insulin and NBM
o Due to nephropathy, poor circulation (atheroma)
o Charcot’s foot/joint
o Deep infection  amputation
 Compartment syndrome – inflammation increases pressure in the deep tissues sufficiently o
cause tissue hypoxia, lead to gangrene, severe deep pain, woody feeling to tissues,
orthopedic review
Radiology
Limb
 2 views, 2 joints, 2 limbs, 2nd opinion and 2 X-ray (another after 1 week)
o Lateral and AP
o Above and below joints
o Compare L to R
 FRACTURE TYPES – transverse, oblique, spiral, compression, comminuted, segmental, intra-
articular (joint), buckle (greenstick), avulsion (tearing off limb), stress fracture
 When commenting note
o Displacement (distal to proximal)
o Angulation (valgus (leaving)/varus (returning)
o Shortening
o Rotation
 Open or closed
 Look for joint effusions
 Monteggia = radial head dislocation with ulnar shaft fracture
 Joint alignment and joint spaces, cortical outline, soft tissue – lipohaemoarthrosis
 ELBOW (check radiocapitellar line and anterior humeral line)
o Fat pads – raised lateral view
o Cortex of radial head smooth on both views
o Radiocapitellar line normal
 MRI – picks up oedema, think there is a fracture but you can’t see it
 CT – to spot fragments, can see fracture on X-Ray
 Reperform x-ray to pick up bone growth 1 week after
 Colle’s fracture = fall on out-stretched hand
 Smith’s fracture = fall with hand inwards
CXR
 Checks initially – name, gender, age, markers (L/R), projection (AP or PA)
 Rotation – medical clavicles equidistant from spinous processes
o Density of lung rotated towards is more lucent
 Penetration - can see vertebrae trough heart shadow
 Inspiration – hemidiaphragms at 6th anterior rib
 NB DENSITIES
o Gas – fat – soft tissue/fluid – bone/calcification – metal
o NB defib leads are thicker, and pacemakers thin
 Cardiac border –
o Cardiothoracic ratio
o L higher to R hilar
o 3 lobes on R and 2 on left
 Hilar
o R shows right interlobar artery, L shows distal LPA and left descending pulmonary
artery
o Arteries radiate out, veins in
o Look for V – hilar point should be 1cm higher in L to R
 Diaphragm – R higher than L due to liver
 Systemic analysis – trachea, mediastinum, heart, CTR, diaphragm, lungs, hilar, vessels, soft
tissue and bones and review areas
 REVIEW AREAS
o Apices
o Hilar
o Behind heart
o Under diaphragm
o Breast shadows
 Opacification can be in the air spaces (bronchioles/alveoli), interstitial or airways
 AIRSPACES = fluffy/blobby, ill-defined, merge, segmental/lobar, air bronchogram,
consolidation
o Pneumonia = infective
o Consolidation can be blood, pus, water, protein, cell debris
 ACUTE
o Pulmonary oedema – cardiogenic v non-cardiogenic, initial interstitial opacification,
spills into airspaces
o ARDS – increased vascular permeability from lung injury, sepsis, trauma, shock,
burns, aspiration, drugs, 12-24 hours lag of CXR to clinical sx, consolidation,
progresses to fibrosis
o Infarct/hemorrhage – pulmonary renal syndromes or PE, infection, trauma,
anticoagulation
o Aspiration – depends on what, gastric acid causes pneumonitis
o Pneumonia – infective, organizing, eosinophilic
 HIV – PCP, infection, fever, cough, hazy, bilateral – airways
 Fat can deposit between ribs and lungs and around mediastinum
 Chronic – lymphoma, adenocarcinoma, sarcoid, lipoid pneumonia, alveolar proteinosis
 Silhouette sign – absence of silhouette, obliteration of heart, mediastinal or diaphragmatic
contours by adjacent opacity
o R heart border = middle lobe
o L heart = lingual
o Lower lobes – hemidiaphragm
 Lobar pneumonia – large part of lobe, oedema, exudate, homogenous or patchy, air
bronchogram
 Bronchopneumonia – pneumonia with bronchitis, mucous plugging/volume loss, ill-defined
nodules, multi-focal and patchy
 Bronchitis – inflammation of the lining of the bronchi, thickening of bronchial walls
(peribronchial cuffing)
 Bronchiectasis – abnormal dilatation of the bronchial tree, large irreversible, causes can be
post-infective, congenital, cancer, foreign body, fibrosis
o On CXR – tram track opacities, signet ring sign, air fluid levels
 INTERSTITIAL = linear/reticular, septal lines, fibrosis, cells or fluid
o End-stage fibrosis, honey combing, reduced lung volumes, architectural distortion
 Interstitial lung disease can be infective, inflammation, fibrosis
o Idiopathic pulmonary fibrosis – peripheral, subpleural reticulation (honeycombing),
volume loss, bronchiectasis, shaggy heart/diaphragmatic contours
o HP
o Sarcoidosis
o CTD
 NB once fibrosis is established it is associated with volume loss
 Pulmonary fibrosis – shrunken lung bilateral opacification, reticular, interstitial oedema,
honeycombing
 COLLAPSE – can be obstructive (tumour, mucous, FB), compressive (pleural fluid,
pneumothorax, adjacent mass lesion) or cicatrisation (fibrotic = TB, radiation, pulmonary
fibrosis)
 Loss of borders = where collapse is
o R mediastinum – RUL = volume loss, horizontal fissure and R hemidiaphragm move
up, tracheal deviation, reverse S sign with hilar bulging
o R heart – RML = obliterates R heart border
o R diaphragm – RLL = loss of R hemidiaphragm, volume loss (usually with middle lobe)
o L heart – L lingual = collapses anterior, small L hemithorax, veil like, tracheal
deviation, L hilar higher
o L diaphragm – LLL = volume loss, elevated and silhouetted L diaphragm, opacity
behind heart (sail sign), can’t see aorta
 Hilar abnormalities = vascular (smooth eg in pulmonary arterial HTN) or nodal or
lymphadenopathy
 White out = collapse, effusion
 Pleural effusion = transudate (low protein) = failures, exudate (high as in infection, PE,
cancer, trauma)
o 200-300mls opaque meniscus at costophrenic angle
o 2 l = moderate
o 5l = white out
o Lamellar – tracks laterally up wall
o Encysted – loculation
 Black lung – rotation, mastectomy, scoliosis, pneumothorax, emphysema, PE
 Pneumothorax –
o Primary, spontaneous, skinny men, 20-40years
o Spontaneous, secondary – COPD
o Others due to trauma, lung biopsy
o TENSION
 Asthma - airway inflammation, reversible airway obstruction and hyper-reactivity to various
stimuli, on CXR can show hyperinflation, flat diaphragm, bronchial wall thickening
  Asbestos – pleural effusion, pleural plaques, asbestosis, lung cancer, mesothelioma
 COPD – obstructive airway disease, chronic bronchitis with emphysema
o CXR sows lucency, hyperexpanded chest, flat hemidiaphragms, small heart, whispy
vessels, bullae, chronic bronchitis would show coarse bronchial
markings/dilated/nodules if mucous plugs
 Sarcoidosis – multi-system non-caseating granulomatous disorder, unknown aetiology, 20-40
years, often black females, thoracic involvement with skin, eyes, liver, spleen, CNS and heart,
also present with fever, malaise, uveitis, arthralgia, weight loss, dry cough, SOB,
hypercalcemia
o CXR can be normal or staged from calcification of nodes to pulmonary fibrosis
 TB – mycobacterium tuberculosis, aerobic bacillus, affects lungs mostly but spreads via
lymphatics allowing multiorgan dissemination – cough, weight loss, SOB, Mantoux (must
amount a response)
o Primary – consolidation, calcification (Ghon)
o Post-primary – reactivation – active disease, cavitation, effusion, adenopathy,
scarring fibrosis
o Miliary – poor immune response – micronodules, widespread
o Reactivation – increasing soft tissue, consolidation, cavitation
 NODULES = causes include military TB, carcinomatosis, lymphoma, sarcoidosis
o Neoplastic
o Infection
o Immunological
o Inhalation
o Vascular
 Heart enlargement – LV boot shape
 Pulmonary oedema – cardiomegaly upper lobe venous diversion, septal lies, peri-bronchial
cuffing, airspace opacification, effusion, consolidation  effusion, kerley B lines
 CF = ring shadows, apical thickening, worse in middle of film
 Lines and tubes – CVC lines (subclavian, jugular), Ng tube, pacemakers
o Pacemaker single lead to RA
o Dual lead to RA and RV
o Three lead/biventricular, Ra and RV and LV for coronary sinus
o Internal jugular or subclavian – central line
Stroke/TIA
 TIA under 24 hours – vision (homonymous hemianopia), speech (dysphasia, dysarthria),
motor/sensation
o ? amiorosis
o Cholesterol (aim under 35), fasting lipids, glucose
o ECG for AF
o ABCD2 – age over 60, BP high, clinical, duration over/under 60 minutes, diabetes – 2,
7 and 90 day risk of a stroke
 Tx of TIA – NOAC if AF, apixaban, scan is unsure of TIA, aspirin 300mg for 2 weeks,
clopidogrel 300mg
 Stroke – CT – 20% hemorrhage, 50% ischaemic
o NB paresis = weakness, plegic = no power
 MCA stroke – contralateral weakness/sensory loss F>A>L, expressive dysphasia/neglect,
homonymous hemianopia
o TACS 3/3, 4% alive at 1 year with 100% morbidity, 2/3 PACS, cardioembolic often AF
 Lacunar – HTN in small vessels, in situ, cerebral amyloidopathy – can be pure sensory, pure
motor, mixed or ataxic hemiparesis (normal power and tone but abnormal movement)
  PCA
o Cerebella
o Occipital
o Brainstem (bilateral CN, pons 5-8, MRI for MS if young)
 Aspirin 200mg 2 weeks
 Haemorrhagic transformation – big territory
Inflammatory Bowel Disease
 Immune response against GI tract – 2 main peaks early adult life (16-30) and late middle life
(55-65)
o NB mesentery is an organ, metabolic organ
o Crohn’s and UC – relapsing and remitting, immune, genetically susceptible host and
trigger
 Ulcerative colitis – idiopathic chronic inflammatory disorder of colonic mucosa, extra
intestinal inflammation, extends proximally from and verge in an uninterrupted pattern to
involve all/part of the colon
 Crohn’s – idiopathic chronic inflammatory disorder of full thickness of the intestine, mostly
ileum and colon, can be anywhere any level from mouth to anal/perianal region, patchy
disease, intervening areas of normal mucosa
 KEY POINTS
Ulcerative Colitis Crohn’s Disease
Th2 – humoral, IL4, 5 and 13 Th1 – cellular, TNF alpha, INF, IL 1, 2, 6, 8 and 12
Worse in non-smokers Transmural
Crypt abscesses, goblet cell number decrease, crypt Non-caseating granulomas (giant cells), skip lesions
distortion Worse in smokers
Complications in gut and liver Complications everywhere else
Bloody diarrhea, abdominal pain (cramping), fever, Strictures and fistula, abnormal connection of 2
tenesmus (race to toilet and can’t go) mucosal surfaces
M:F = 2:1 M:F = 1:1
Abdominal pain, perianal disease, weight loss,
obstruction from fistula, malaise, anaemia bloody
diarrhoea
 NB granulomas seen in = TB, sarcoid and CD
 Investigations
o Blood tests – anaemia, B12, folate (terminal ileum for B12), low albumin
o Faecal calprotectin – for IBD
o Capsular endoscopy
o In UC colonoscopy for pre-malignant polyps, 8 years post diagnosis
 OTHER COMPLICATIONS (osteoporosis, infertility, cancer)
o Erythema nodosum – on shins discrete, red, painful lumps
o Pyoderma gangrenosum – red patch, ulcerates, black, gangrene and pus
o Sero-ve polyarthritis – ankylosing spondylitis or little joints or big joints
o Iritis – anterior uveitis, exudates, red eye, acutely painful, reduced vision, eye shape,
steroid drops
o Episcleritis – bright ted and painful, steroid drops
o Calculi
o Pyelonephritis
Ulcerative Colitis Crohn’s Disease
Dilatation – toxic megacolon, over 6cm diameter, Ischaemic colitis
distended, painful Bechet’s disease
Perforation Drugs (diclofenac/NSAIDs)
 Peritonitis Appendicitis
Irritable bowel syndrome Infection
Infection Obstruction
Tumour/cancer Adhesions
Diverticulitis 80% small bowel
Coeliac disease Abscesses
IN gut AND LIVER Faecal incontinence
Sclerosing cholangitis (increases risk of cancer) Mouth ulcers
Systemic amyloidosis
 Treatments are varied
o 5-ASA – inhibit COX2, used in UC, acute flares and remission, safe in low risk
interstitial nephritis, prevents bowel cancer, SE headache, diarrhea
o Steroids – food for exacerbations, huge SE profile
o Immunosuppressants
 Azathioprine, 6-mercaptopurine, methotrexate – (first 2 in pregnancy)
 For remission, prevent CD structuring, deranges LFTs, skin cancer risk
increases, pancreatitis
o Biologics – antibodies eg TNF alpha, infliximab, not safe risk of infection and
lymphoma, good in crohn’s, but decreasing effectiveness and expensive – use anti-
TNF if steroids fail
o Elemental diet – crohn’s in children
 Surgery
o UC – if medical treatment fails, take colon out, subtotal colectomy, pouch formation,
increase bowel habits
o CD – remove as little as possible, crohn’s occurs at anastomoses, short bowel issues,
not curative, 70% have bowel symptoms
 SEVERE ATTACKS
 Also consider bacterial infection, viral infection (immunocompromised), amoebic dysentery
ischaemic bowel and diverticulitis
 UC – more than 6 episodes of bloody diarrhea, pyrexia, tachycardia, raised inflammatory
markers, bowels opening at night, albumin below 30 and Hb below 10
o Treat with steroids (prednisolone enemas, IV hydrocortisone)
o Early senior review
o Send off stools (stool chart)
o Bloods – FBC (anaemia, infection), U&E (dehydration, electrolytes (low K/Na), LFTs,
albumin), blood culture
o Abdominal X-ray – perforation, cobble stoning, toxic dilatation
o CXR – erect for perforation
o Biopsy – flexi sig
o After 3 days take out colon
 Crohn’s flare presents with diarrhea, abdominal pain, fistula, obstruction, abscesses
o As above but…
o AVOID surgery – treat with biologics
COPD
 Common, smoking, chronic bronchitis (persistent cough for 3/12 for 2 years) and
emphysema (loss of elasticity, dilatation of distal airways)
o ?? alpha 1 anti-trypsin deficiency
 NB CF – bronchiectasis, whooping cough, tumours, sarcoid, pneumonia recurrent
 History – smoking, cough, chest infections, SOB
  Examination – nicotine, hyperexpansion of chest, increased accessory muscle use, mild CO2
tremor, check lips for cyanosis, auscultation (wheeze)
 Spirometry
Obstructive Restrictive
FEV1  
FVC  
FEV1/FVC  
 COPD – high residual volume and high total lung capacity
o NB asthma, normal residual volume and normal total lung capacity
 TLCO – transfer factor
 Va = alveolar volume
 TCo – transfer co-efficient – indication of how effectively gaseous exchange is occurring –
considers effective alveolar surface (surface area integrity), Hb concentration and V/Q
matching
o Reduced in emphysema, fibrotic lung disease and pulmonary oedema
o Increased in asthma, sarcoidosis, pulmonary haemorrhage
 Only increased in vasculitis/haemorrhage
 Pulmonary Fibrosis – asbestosis, ankylosing spondylitis, amiodarone, IPF, TB, radiation,
sarcoid, methotrexate use
 Restrictive – low TLC, low transfer factor, small residual volume
o CXR – pneumonia, pneumothorax
o ABG – hypoxia, acidaemia
 ACUTE COPD – 88-92%, hypoxic drive, controlled by oxygen, steroids, CXR, nebulized
salbutamol (2.5mg B2B), ipratropium, ABG, antibiotics (doxycycline/co-amoxiclav)
o CAP – h. influenza, Moraxella, strep penumoniae
o Bronchitis – viral, fever, sepsis, sputum, colour, amount purulence
 Treatment COPD – inhalers or nebulisers
o Conservative – stop smoking, optimise BMI, environmental (smoke outside),
increase exercise, decrease intake, healthy lifestyle, self-directed or physio graded
o Medical – salbutamol (b2 agonist), long acting anti-muscarinic (tiotropium), long
acting B2 agonist,
 Steroids – FVC under 50%, inhaled if 2 or more exacerbations/year
 3 in 1 inhaler
o Mucolytics – carbocysteine
o Theophylline/aminophylline
o Long term oxygen – PaO2 under 7.3, when well, or 7.3-8 if R sided HF
 Rescue packs are used with antibiotics and oral steroids for exacerbations
 Stop smoking
o Champix
o Nicotine
o Supportive – psychological, support groups
 CHRONIC T2 RF
o NIV
o BIPAP
Ventilation
 End expiratory pressure higher in COPD, intrinsic PEEP –
improve with pursed lips, posture (tripoding), barrel
chest, to decrease intrinsic PEEP
 In exacerbation this gets worse – push in expiratory PEEP higher than intrinsic PEEP
o IPAP(Co2 dependent) higher than ePAP (O2 dependent)
 o BiPAP – tidal volume needed to get rid of CO2
 Non-invasive ventilation – pH worse
Respiratory Failure Revision
 T1RF – hypoxaemia, PaO2 of under 8 on air
o Restrictive – fibrosis
o T2RF – hypoxaemia with hypercapnia, respiratory depression, hypoventilation,
ankylosing spondylitis, COPD, opioid/benzo OD, bronchiectasis, MND,
neuromuscular, vasculitis, obesity, MS
GI Bleeding
 Preparation, triage, ABCDE, resuscitation – blood, cross match, IV access, VBG, secondary
survey, monitor and re-evaluate
o Anesthetics, ITU
o Shock – unable to perfuse tissues
 History – BP, pule, temperature
o Melaena = black sticky, tar stool, partially digested blood, NOT clots or fresh blood
 UGI bleed – Mallory Weiss tear, varices, peptic/duodenal ulcers, oesophagitis, GAVE, GIST,
oesophageal/gastric cancer, gastritis, deranged clotting, angiodysplasia
 Management
o IV access, 2 large bore cannulae
o Bloods = FBC, U&E, LFTs, group and save, clotting  maybe low Hb, high urea
(digested blood, LFTs deranged (high bilirubin, low albumin)
o Blatchford or rockfall – Risk stratification – urea, Hb, systolic BP, others
o Erect CXR
o VBG/ABG – lactate, compensation
 SHOCK
o 15% blood loss, minimal tachycardia, BP/RR normal
o 30% blood loss 1.5l, high HR and RR, low p pressure
o 30-40% - 2L, fall in systolic BP, and conscious level
o 40% - high HR, systolic BP, normal pulse pressure, clammy, cold pale
 NB beta-blockers can mask tachycardia
 RESUS – fluids, cross-match for bloods
o Varices – antibiotics, terlipressin 2g QDS
o PPI infusion – omeprazole 40mg every 4 hours
o Platelets nder 50 – replace
o Transfuse if Hb under 70g/l
o Antibiotics = ceftriaxone 2g IV OR ciprofloxacin 500mg IV
o ?tranexamic acid
o Senior review – endoscopy, ITU
 Post-endoscopy – 72 hours PPRI infusion, H pylori testing, home on PPI
 Lower GI bleeding – maroon/bright red
o Causes include – diverticulitis, tumour, haemorrhoids, colitis, over anti-coagulation
o Attend to blood loss, correct coagulopathies, do not normally scope – CT SCAN
 Treatments
o Clip/cauterizes, adrenaline for ulcers
o Band varices
o Duodenal oversew surgery
o Therapeutic angiogram – uncontrolled duodenal bleed
o Stent – tube, balloon (variceal bleed), embolic, ischemia
o TIPPS – liver, decrease portal pressure
Communication TOP TIPS
  Apologise
 No promises
 Repeat phrases
 Hospital complaints – PALS
 Active listening
 Explain situation – no medical jargon
 Empathize – sign posting
 Speak clearly
 Difficult conversations – medical reg/consultant
 Mistake – document in notes, online form, inform patient, given them time to ask questions,
tell senior – complete honest – human error
 RSVP
o R – reason – for communication and patient attendance
o S – story – key elements of history significant PMH
o V – vital information – clinical finding, test results, EWS, treatment, working
diagnosis/problem list
o P – plan – outstanding investigations/results, outstanding treatment/procedures,
destination, patient information, additional considerations
Pneumonia
 Risk factor – immunosuppression/immunocompromised, elderly, smoking, structural (CF,
COPD, bronchiectasis), alcohol (if U60 then need HIV testing)
 CURB 65 – if 0-1 then manage at home, 2 clinical judgement and 3 or above then admit,
hospital admission, mortality 15%
o Confusion – AMTS 8 or below
o Urea (over 7)
o Respiratory rate (over 30)
o BP (systolic under 90 or diastolic under 65)
o 65 – age over 65
 Signs/symptoms – fever, sweats, malaise, SOB, haemoptysis, cough, productive, phlegm,
chest pain (pleurisy), parietal pleura for pain, sharp stabbing pain
 Travel history – atypical symptoms eg unwell with abdominal pain, no cell wall of organisms,
wont be treated with penicillin, may need macrolide, need bloods, CXR and sputum sample
o Atypical = mycoplasma, legionella, chlamydia (serology needed), Moraxella
o ? if safe swallow
o Legionella – water, air conditioning, notifiable disease
 Typical= pneumococcal, staph/strep and HIB
 Typically will show high WCC, platelets, urea, creatinine (sepsis -> AKI), high CRP, blood gas,
cultures (only show 10%), deranged LFTs
o CAP = amoxicillin
 Resolution
o Clinical cure – feels better in a few days
o Radiological cure – 6-8 weeks
o Microbiological cure
 Complications
o Exudative effusion (pleural)
o Empyema – culture/pH 7.2 or below (treat with drain), pus in closed sac, poor
prognositically, drain, pockets, surgical drainage, loculated
o Lung abscess – prolonged antibiotics (6 weeks)/surgery
 HAP – different bugs, poor prognosis, gram -ve, tazobactam with pipercillin = TAZOCIN
 Aspiration pneumonia – anaerobes, gram -ve, metronidazole
  TRANSUDATE V EXUDATE
o Transudate – systemic, HF, kidney failure, often bilateral
o Exudate – local
 Lights criteria – LDH (Serum), protein over 50% = exudate, LDH more than 2/3 of range then
exudate
HEART FAILURE
 Causes – HTN, ischaemic heart disease, endocarditis, genetics, cardiomyopathy, toxins,
inflammation
 Symptoms – SOB, oedema, orthopnoea, fatigue, syncope, palpitations, PND, pre-syncope,
TOI
o Bibasal crackles, murmur, JVP, hepatomegaly, oedema
 REF – under 45%
 PEF – normal over 55%
 Investigations
o Cardiac imaging – cardiac MRI, 3D assessment
o CXR – cardiomegaly
o Co-morbidities – HTN, DM, HF, HCM, AS, endocarditis, amyloidosis, sarcoid
o Bloods – CRP, clotting, trop, FBC, ferritin, LFTs, folate, TFTs, U&E
 Management
o HEFPEF – spironolactone/furosemide – no increase in m/m but symptomatic relief
o REF
 ACEI – inhibit RAAS, Ramipril, CI poor renal function, high K and low Na
 Diuretics – mostly loos, furosemide (40mg)/bumetanide 1mg
 B-blockers – bisoprolol – CI bradycardia, BP, asthma, not in acute pulmonary
oedema
 Poor heart output – spironolactone, K+ diuretic, MRA
 Cardiac resynchronization therapy, under 35%, pacemaker for HF
o ECG sowing BBB (QRS over 120ms)
o 3 leads – RA, RV, coronary sinus LV
o Either
 Standard CRTP pacemaker
 CRTD defibrillator
Diabetes Medication
 Biguanides – metformin
o Multi-action, decrease CV complications, weight neutral, no hypoglycaemia
o Bad in AKI, creatinine 150, lactic acidosis
o STOP in sepsis, MI, stroke and contrast 48 hours
o GI SE
 Sulphonylureas – gliclazide, avenclamide
o Hypoglycaemic agent, acts on B cells, take BD with food
o Stop if not eating – sick, elderly
o Not for the old frail patient
o Renal excreted – do not use in AKI/high creatinine
 DPP4 inhibitor – gliptins eg saxagliptin
o Does not cause hypoglycaemia, weight neutral, excreted by liver
o Do not use in pancreatitis
o Linagliptin 5mg OD, regardless of renal function
 SLGT-2 inhibitors – dapagliflozin
o Promotes glycosuria from kidney
o Increased risk of UTI/thrush
 o Do not cause hypoglycaemia
o Use up to eGFR of 45
o Dehydration, lose weight, decreases risk of stroke and MI
 Thiazolidinediones – pioglitazone
o Once daily, no hypoglycaemia, weight gain, exacerbates HF
o Osteoporosis and bladder cancer
 Non-insulin injectables
o GLP-1 – exenatide, loraxatide, for post-prandial BG, eGFR of 30
o OD or BD or once weekly
o Weight loss
o GI SE nausea etc
o Do not use in acute pancreatitis
 NB INSULINS – 30% short acting usually
 Sliding scale
o T1 – 0.1-0.2 units/kg/day
o T2 – 0.5units/kg/day
AMU teaching extras
 DKA – ABDCE, 500ml NS bolus, start insulin, bloods, ketones, dipstick, potassium
 AF
o Rate control
o Rhythm – if cardiac unstable
 Medical – flecanide
 Electrical – DC cardiovert (usually 1 month later)
o Anti-coagulate
o ECHO – clot formation, LA dilatation
o Refer to cardiology
 Causes of AF infection, TFT, mitral valve issues, dehydration, alcohol, IHD, cardiac issues
 UGI bleed – catheter, protect airway, ABCDE, IV access, fluid boluses, cross match, bloods,
history (NSAIDs, alcohol), IV PPI, endoscopy, fluid balance, stool chart, repeat obs,
terlipressin, antibiotics,
clotting, IV PPI
Liver Disease
 Liver function tests
o Measures of
synthetic function
o Inflammation
 Synthetic function
o Albumin
o INR
o Platelets
o Bilirubin
o ALP
o ALT/AST
o Gamma-GT
 Post-hepatic/Obstructive – blocked bile duct = stones or cancer
(pancreatic/cholangiocarcinoma), structures, lymphoma  will see ALP>ALT
o Stones – painful RUQ, colicky, septic, rigors, USS
o Cancer – painless jaundice, mass palpation, weight loss, new onset DM, high calcium
(19-9)
 Investigations – CXR, blood cultures, USS, bloods, obs, CR scan/MRCP (staging pancreatic
cancer or USS -ve), drug history important for jaundice
o ERCP – interventional, remove stones, not diagnostic
o Endoscopic USS – good for staging pancreatic cancer
 Treatment
o Stones – ERCP, cholecystectomy, exploration on bile duct
o Cancer = staging, stent to relieve jaundice (via ERCP/percutaneous stent), WHIPPLES
to remove, give creon (pancreatic enzymes)
 Intra-hepatic jaundice
o Alcoholic fatty liver disese (most common
o Hepatitis (viral)
o NAFLD
o Autoimmune
o Others include drugs, cancer, cirrhosis, ischaemic injury
 Investigations – USS with dopplers, history important (COCP thrombosis in liver), LFT, FBC
(platelets, thrombopoietin, low platelets), MCV (chronic macrocytosis in alcoholism), INR,
hepatitis serology (A and E, EBV and CMV), autoimmune, immunoglobulins, ferritin,
caeruloplasmin (haemochromatosis, Wilson’s disease for copper), paracetamol, salicylate
levels
 VIRAL HEPATITS
 A and E  faecal, oral, gut infections
o A – raw shellfish, self-limiting, incubation 4-6 weeks
o E – liver failure, more common, pregnancy, fulminant in pregnancy can lead to
transplant
 B – DNA virus, Africa/asia, sex and drugs, IVDU/sex workers at risk, incubation 30-160 days
o HBsAg – antigen, current infection
o Anti-HBs – immunity
o IgM – recent/reactivation – ACUTE
o IgG – remote infection – PAST
o Viral DNA (active replication)  immune tolerant phase (persists till 40yrs, high HBV
DNA, normal ALT)  HbeAg +ve chronic, active inflammation/fibrosis with liver
damage and raised ALT  Inactive carrier no further damage  HBeAg -ve, more
injury
o If child then chronic infection, maternal-fetal route
 Hepatitis B infection – treatment, active replication/infection, INTERFERON/ADENOVIR –
reduced inflammation and infectivity
 Hepatitis C  RNA virus, incubation under 30 days, IVDU, chronic infection, high HCV RNA
and anti-HCV antibodies
o Treatment with combination therapy
 Autoimmune hepatitis – chronic with acute flares, F more than M, without treatment leads
to cirrhosis, non-specific symptoms of RUQ pain, jaundice
o Investigations with ANA and SMA (+ve anti-smooth muscle antibody specific to
autoimmune hepatitis), +ve LKM-1
o 20% no antibodies
o Lymphoplasmacytic infiltrate, bridging necrosis, prominent interface hepatitis
o Treatment similar to IBD, steroids and azathioprine for 5 years before weaning
 Primary biliary cirrhosis – autoimmune, chronic, destruction to small bile ducts, cholecystitis
 fibrosis  cirrhosis, AMA +ve with lymphocytes, granulomas and periportal fibrosis
o Management with ursodeoxycholic acid, monitor cirrhosis (OGD varies 6 monthly
USS), cholestyramine for itch
  Sclerosing cholangitis – autoimmune, big bile duct, in and out of liver, many have UC,
beading on MCRP/structuring, onion skin, ANCA +ve
o Management with ursodeoxycholic acid, cholestyramine, stent bile duct
o High risk of cancer of bile duct and colon – screen yearly with colonoscopy
 Fatty liver disease – high due to obesity, very common cause of cirrhosis, NASH – metabolic
syndrome, systemic condition, main treatment is weight loss
 Hepatorenal syndrome – correctable factors eg dehydration, sepsis, shock, poor prognosis,
discontinue nephrotoxic drugs, human albumin solution and terlipressin (vasopressor)
 Cirrhosis – variceal bleeding, cancer, follow up important
Drugs and the liver
 Antibiotics
 Anti-epileptics
 Cardiac drugs – STATINS
 OTC
 Idiosyncratic reactions – time course delay of 90 days
 Presentation = hepatitis, cholestasis, steatosis, fibrosis, cirrhosis
o Hepatocellular (high ALT)
o Cholestatic (obstructive) (high ALP)
o Mixed
 ANTIBIOTICS
o Augmentin – seen 8 weeks post use, 1 week hepatocellular and after 2-3 weeks
cholestatic picture
o Nitrofurantoin – hepatocellular, immunological, rare/unpredictable, lupus like, stop
drug, autoimmune hepatitis
o Erythromycin – cholestatic, 1-3 weeks post use
o Flucloxacillin – 3 weeks post treatment
 ANTI-EPILEPTICS – deranged LFTs
o Phenytoin – acute hepatits, within 6 weeks
o Carbamazepine – cholestatic
o Sodium valproate – hepatic
 CARDIAC
o Amiodarone – lipophilic, safe in all arrhythmia, deranged LFTs
o ACEI – unlikely
o STATINS – asymptomatic rise in ALT in 12 weeks, start on statins even if high ALT –
NAFLD
 Paracetamol – more than 75mg/kg sufficient, risk factors include alcohol, malnourished,
enzyme inducers, blood gas shows metabolic acidosis, paracetamol/INR, salicylate, FBC,
U&E, LFTs
o Severe poisoning = INR over 2 in 24 hours and over 6 in 72 hours, hypoglycaemia,
renal failure, metabolic acidosis (pH under 7.3), encephalopathy (neuro obs), high
lactate over 3, fluid resistant hypotension  transfer to tertiary center
o Paracetamol level at 4 hours, NAC if 8 hours of injection, care if staggered doses
 Alcohol – alcohol dependency
o Acute alcoholic hepatitis – inflammation, potentially reversible, jaundice, confusion,
ascites, encephalopathy, deranged clotting, low albumin, high bilirubin and platelets,
co-existing sepsis (atypical), full septic screen, USS liver and doppler, ECHO if IVDU,
tap ascitic fluid, nutritional support, stop diuretics, steroids (decrease inflammation
if NOT septic) prednisolone 60mg OD
o GASH score – child-pugh score
 Ascites – diagnostic tap (cytology), cancer or liver failure
 o Systolic blood pressure with ascites high mortality
o More than 250cells/mm^3 – neutrophil count
o If tense drain, fluid restrict, diuretics (once LFT at baseline then spironolactone up to
400mg a day), decrease salt in diet, TIPPS
 Encephalopathy – graded 1-4, EEG, treat cause, laxatives (lactulose) with rifamixin
Joint Examination PowerPoint
 General joint examination – look, feel, move, special tests
 Shoulder
o Anatomy – humerus, scapula, clavicle, labrum (cushions head of humerus in glenoid
fossa), bursa (allows smooth movement of muscle), acromion, intrinsic muscles =
Deltoid (abduction), teres major and rotator cuff, extrinsic = levator scapulae,
rhomboid minor and major, trapezius and latissimus dorsi
o Rotator cuff = for stability and rotation
 Supraspinatus
 Infraspinatus
 Teres minor
 Subscapularis
 Shoulder examination -
o Look – anterior, posterior and lateral, asymmetry in shoulders, position of arm, bony
prominences, scars, bruising, swelling, muscle wasting, lymphadenopathy, shoulder
blades
o Feel – temperature, pain (septic arthritis, inflammation), palpation – sterno-
clavicular joint, along clavicle, AC joint, coracoid process, humerus and along scapula
 Axillary nerve – over deltoid
o Move – grossly with hand on head (abduction and external rotation) and hands on
small of back (adduction and internal rotation)
 Active – flexion (180), extension (40), abduction (180), adduction (30),
external rotation (80), internal rotation (up to T4-T8)
 Passive – crepitus (OA)
o Special tests
 Supraspinatus, resistance against abduction 30 degrees, tendonitis/weak
 Infraspinatus and teres minor – external rotation against resistance, boxer
 Subscapularis – small of back and push back, internal rotation
 Painful arc (between 60-120) for impingement of supraspinatus, passive up
and down slowly
 Serratus anterior – winged scapula, push against wall
 Shoulder apprehension for instability - sublaxity
 ACJ scarf test
 Common shoulder pathology
o Impingement syndrome – supraspinatus inflamed due to impingement below
acromion, painful arc, tx with physio, analgesia and steroid injections
o Rotator cuff tear – muscle tear, many times, impingement syndrome, weakness in
abduction and supraspinatus wasting, treatments from conservative to surgery
o Frozen shoulder or adhesive capsulitis, idiopathic adhesions, severe pain and
stiffness, loss of active and passive movement in all directions, physio to maintain
movement, steroid injections
o Tendonitis
o OA - crepitus
 Elbow
 Hands
 Hip – femur and pelvic acetabulum, muscles = iliopsoas,
gluteal muscles, adductors, piriformis, rectus femoris,
sartorius and hamstrings
 Hip Examination
o Look – standing, assess gait, muscle wasting,
scars, swelling, bruising, sitting – muscle bulk,
measure true and apparent
o Feel – temperature, bony landmarks (greater
trochanter (trochanteric bursitis) and pain in
groin), general palpation around hip joint
o Move – flexion, internal and external rotation,
abduction, adduction and extension (in prone
position)
o Special tests
 Thomas test – patient flat, hand under
lumbar spine, raise/flex hips, move opposite leg down, should fully extend
hip
 Trendelenburg – abductor – stand on one leg, dip to the opposite side of the
muscle weakness  normally contralateral side will raise
 Knee – femur, tibia and patella, anterior and posterior cruciate ligaments and medial/lateral
collaterals, menisci and bursae (x4)
o NB valgus = knock-knees, varus = bow-legged
o Common – total knee replacement
 Knee Examination
o Look – assess gait (limp, movement restriction, crutches), anterior (scar, swelling,
muscle wasting, asymmetry, valgus/varus deformity), posterior (popliteal swelling =
bakers cyst), hyperextension
o Feel – lie on couch, temperature, quadriceps bulk (20cm above tibial tuberosity),
palpation (top of patella, fell along sides, into joint space, into ligament insertions,
posterior popliteal fossa), patellar tap and effusion sweep
o Move – flexion and extension (active and passive), hyperextension (raise leg by heel)
o Special tests
 Anterior/posterior draw test (ACL/PCL laxity), tibial tuberosity, push (PCL),
pull (ACL)
 Medial/lateral collaterals – force on tibia
 McMurray for meniscus tear
 Medial – external rotation of foot and abduction of hip
 Lateral – internal rotation with adduction of hip
 Pathology of the knee
o OA
o Knee replacement
o Bakers cyst – weakness in synovium, synovial fluid leak, can drain but can return
 Spine anatomy – 7 cervical, 12 thoracic, 5 lumbar and sacrum, spinal cord terminates L1
(becomes cauda equina)
 Spine Examination
o Look – assess gait, inspect posterior and lateral for posture, asymmetry, scoliosis,
hair growth, café au lait spots, muscle wasting, lordosis and kyphosis
o Feel – temperature, palpate along spinous processes, feel along paraspinal muscles,
palpate sacroiliac joint
 o Move
 Cervical – flexion/extension (chin to chest to ceiling), Lateral flexion (cheek
to ear), rotation (chin to shoulder)
 Thoracic – sit with arms crossed and rotate chest
 Lumbar – flexion (touch toes), extension (lean back), lateral flexion (slide
hands down side)
o Special tests
 Schober’s – 10m above dimples and 5cm below, when back straight,
remeasure on flexion, increase of less than 5cm is +ve
 Straight leg raise (L4/5-S1), sitting, hip flexion, pain down whole leg is +ve
 Femoral stretch (L2-L4) – patient prone, flex knee and extend hip, pain in
back/anterior thigh (inguinal) +ve
Connective Tissue Diseases
 Autoimmune V Inherited
o Collagen vascular = connective tissue and vasculitis
 Autoimmune connective tissue disorders
o SLE
o Systemic sclerosis
o Idiopathic Inflammatory Myopathies
o Sjogren’s Syndrome
o Mixed CT disease
o Rheumatoid Arthritis
 SLE – multi-system autoantibody production with immune complexes, 15-45 years F>M,
AUTOANTIBODIES (ANA, anti-nuclear, anti-phospholipid, anti-ribosomal P protein  anti-ds
DNA)
o Mouth/nose ulcers
o Skin – butterfly rash, red patches
o Heart – endocarditis, atherosclerosis
o Severe abdominal pain
o Blood – anaemia, high BP
o Muscle and joints – pain, arthritis, swollen joints
o Hair loss, high temperatures, headaches
o Kidneys – blood in urine, nephritis
o Lung – pleuritis, pneumonitis, PE, hemorrhage
o Diagnosis with clinical findings, lab markers, biopsies, history – using SLICC 2012
criteria
o Management – oral prednisolone, DMARDS, biologics (rituximab, belimumab)
 Severe disease – IV methylprednisolone with cyclophosphomide
 Neuropsychiatric lupus – 19 types, with seizure, movement disorders, anxiety/mood
disorders, psychosis, polyneuropathy etc
 Libman-sacks endocarditis = SLE associated endocarditis
 Systemic Sclerosis – scleroderma with internal organ involvement, 45-65 years, F>M (males
have more severe disease)
o Interstitial lung disease
o PAH
o GI symptoms
o Raynaud’s
o Telangiectasia
o Calcinosis
o Digital ulcers
 o ANTIBODIES – define where/severity of disease
 Systemic sclerosis management - depends on symptoms – immunosuppressive, for
kin/vascular/DMARD then organ-based treatment
o Vascular – conservative (keep warm), medical (SSRI, CCB, nifedipine, STATINS,
sildenafil, ARB/ACEI), surgery (botox, debridgement)
o Anti-fibrotic – MTX, ciclosporin, rituximab, IVIg, minocycline
 SARCOID – granuloma formation affecting lungs, skin and LN mostly, can affect eyes, liver,
heart and brain, have high calcium, high levels of ACE, erythema nodosum,
 AMYLOID – amyloid (abnormal protein) builds up in bone marrow and is deposited in body
 diarrhea, weight loss, fatigue, bleeding, numbness, swelling of legs, hepatosplenomegaly,
nephrotic syndrome
 Idiopathic Inflammatory Myopathies (dermatomyositis, polymyositis, inclusion body
myositis, idiopathic immune mediated necrotizing myositis)  F>M
o Proximal muscle weakness
o Cutaneous – papules, photosensitive rash, mechanic hands, allotropic rash???
o Heart – dysrhythmia, myocarditis
o Arthritis
o Pulmonary – interstitial lung disease, pulmonary HTN
o Raynaud’s
o GI – oesophageal dysmotility, rectal incontinence
o Low grade fever, weight loss, fatigue, high risk of malignancy
 Sjogren’s syndrome – anti-Ra, anti-La, dry eyes, mouth, F>M, 40-60 years lymphocytic
infiltration of salivary, lacrimal and exocrine glands  SICCA syndrome with systemic
symptoms including arthritis, raynauds, fever, fatigue, distal tubular acidosis, diabetes
insipidus
 Mixed CT – overlap of SLE, SSC and inflammatory myositis  diagnosed with UI-RNP
autoantibodies
Final Year OSCE Respiratory Revision
 20 cigarettes/day = 1 pack year
 CHEST PAIN – relevant past history – management with ABDCE, obs chart, BP, oxygen (15/L
non-rebreathe), ECG (compare to previous)
o Morphine – 1-10mg titrated to pain
o Oxygen – 15L
o Nitrate – GTN, 2 puffs, sublingually
o Aspirin – 300mg STAT
o Anti-emetic 10mg IV metoclopramide
 Clopidogrel 300mg – hospital protocol, cardiology, guidelines
 Oxford clinical handbook – know doses for emergencies ****
 Pneumonia – patchy consolidation, R mid zone – pneumonia, ABG, blood, CXR, ECG
o CURB-65 score
 Confusion
 Urea over 7
 RR over 30
 BP over 90/60
 65 – age
o Scoring where 0-1 (home/oral, 1.5%
mortality), 2 (9%) and 3-5 (22% - hospital Abx)
 Pleural Effusion
o Transudate = renal, heart or liver failure
 o Exudate – PE, cancer, infection, inflammation, TB
o LIGHT CRITERIA
 ABG – respiratory acidosis, decompensated T2RF
 T2RF
o ABCDE
o Steroids – oral prednisolone 40mg/IV hydrocortisone 200mg
o Ipratropium – 500mcg
o Salbutamol 2.5mg
o Antibiotics/oxygen (88%-92%, venture)
o Non-invasive ventilation – BiPap
o NB CPAP used in T1RF oedema
 UGI bleed – urgent OGD, IV omeprazole 80mg, NBM, fluid resus, catheter (fluid balance),
group and save, cross match
Renal
 Home work – DIALYSIS
 Polycystic Kidney Disease – most common genetic renal condition, presents 30-40, avoid
screening, can lead to end stage renal failure
o Problems include stroke, hematuria, loin pain, anaemia, autosomal dominant
(recessive less common), berry aneurysms (SAH), liver and pancreatic cysts, mitral
valve prolapse
o Can only say NOT if 20-30 and no cysts
 Alport’s – kidney failure with deafness and cataracts
 Tolvaptin = ADH receptor inhibitor, increases diuresis
 HSP – rash, purpura, GN (IgA Vasculitis), abdominal pain
 NB protein creatinine ratio (/ 100 for g)
 IgA nephropathy – most common cause microscopic haematuria, if with proteinuria
(monitor and biopsy), more episodic
o Baseline microscopic  macroscopic post URTI/illness
 Renal tubular acidosis – high or low potassium
 Post-strep GN not common, unwell, 1 episode of nephritic symptoms  URTI leading to AKI,
nephritic with blood and protein in urine with high creatinine
 Minimal change – most common in children
 Membranous GN – most common in adults
 EPO – pure red cell aplasia, HTN (link to stroke)
 FLUIDS – 30ml/kg/day, 12 hourly bag of fluid 83ml/hour
 Acute tubular necrosis – most common cause of AKI, common cases being low BP and
nephrotoxic drugs
Lung Cancer Take 2
 Smoking, asbestos, radiation, pulmonary fibrosis, HIV, heavy metal exposure
 80% non-small cell, squamous cell, adenocarcinoma (not always smoking), bronchoalveolar
 15% small cell – aggressive, SIADH, chemo/radiosensitive
 SIGNS AND SYMPTOMS
o Local – cough, SOB, haemoptysis, pleural effusion, Horner’s, hoarse voice, weak grip
strength, hiccups, elevated hemi-diaphragm, shoulder tip pain, SVC obstruction
(flushed, neck, swelling, headache worse forward), dysphagia, infection, wheeze,
collapse
o Mets – weight loss, back pain, lymphadenopathy, hypercalcaemia (NSC), SIADH, liver
edge, pathological fracture, dysphagia, neurology (brain mets)
 o Paraneoplastic – lambert eaton, limbic encephalitis (personality change, memory
issues), SIADH, Cushing’s syndrome dermatomyositis, polymyositis,
glomerulonephritis
 Investigations – biopsy, CXR, bloods, clotting, CT scan (chest, head, abdo), PET scan, surgery
(mediastinal/thoracoscopy), bronchoscopy (EBUS – LN), spirometry
 Management – surgery, radiation (radical/palliative), chemotherapy (immunotherapy),
supportive care
o USE WHO PERFORMANCE STATUS
 Mesothelioma – asbestos, chest pain, SOB, pleural effusion, thickening, death to coroner
Cardiology
 THINGS TO KNOW
o Syncope
o SOB
o Chest pain
o Palpitations
o AF, fast tachy, HR, ACS
 CRT
 Bradyarrhythmia
o Drug history – rate control, amiodarone, B blockers, ivabradine, CCB, verapamil,
diltiazem
o Diuretics
o Clotting
 Investigations – L/S BP, ECG, HR/BP, bloods (FBC, U&E, clotting TFT), 24 hour tape, ECHO
(ejection fraction, valvular lesions (aortic stenosis), HOCM, cardiomyopathy)
 Collateral history important
 Reveal linq – loop recorder
 Aortic stenosis – syncope, presyncope, chest pain SOB
 Tachy-brady syndrome – fast AF to brady – cardiac device with rate control meds
Glomerulonephritis
 Nephrotic – oedema, proteinuria (3g/24 hours = 300 PCR), hypoalbuminaemia (?
hypercholesterolaemia)  low protein, oncotic v hydrostatic pressure
o Anti-pla2 – antigen mebrane, immune complex, disruption, podocyte effacement
o Diabetes – kimmelstein-wilson lesion??
o Membranous nephropathy – thick membrane, treat with steroids and
ciclosporin/tacrolimus
o FSGS – pinker in areas, fibrosis = pink, treat with steroids, can be idiopathic or
secondary
o Minimal damage – immune, responds well to steroids
 Nephrotic syndrome
o Adults = 1-2 month improvement, 1 membranous nephropathy, 2 FSGS, 3 minimal
change disease (others include diabetes and membranoproliferative
o Children = improve in 1-2 weeks, over 90% are minimal change disease treated well
with steroids
 IgA nephropathy – microscopic haematuria normally but macroscopic when ill
 Membranoproliferative GN – thick membrane with proliferation of cells (inflammatory cells)
o Proliferation  inflammation  glomerulus bursts and inflammatory cells enter
bowman’s space – CRESCENTIC NEPHRITIS
 Nephritic – haematuria, proteinuria (active urine sediment), high creatinine (AKI)
o ANA-antibody, anti-GBM, lupus, ANCA vasculitis, IgA nephropathy, post-infectious
GN, HSP
  Chest X-ray  pulmonary hemorrhage, pneumonia, pulmonary oedema
 RENAL PHYSIOLOGY
Palliative Care Teaching


 Chaplain – spiritual issues – concerns over individual existence, as a person, our capacity as
human beings for self-transcendence (overcoming of limits), relationship, love, desire,
creativity, altruism, self-sacrifice, faith and belief
 Ascites – 5L or more then drain over 24 hours
o Serum albumin:albumin 1-1.1
o Over 1.1 = transudate, cirrhosis, hypertension, portal HTN, LF/HF
o More in ascitic fluid in cancer/infection
 Hiccups – involuntary spastic contraction of diaphragm and intercostal muscles leading to
inspiration of air, followed by the abrupt closure of the glottis
o Peripheral causes – GI and non-GI – irritation of diaphragm/phrenic nerve
o Central – medullary stimulation – raised ICP, MS, PD
o Others – electrolyte imbalance/alcohol/stress/medication
o Management – TREAT CAUSE eg PPI, sipping cold water, breath holding,
dexamethasone, gabapentin
 Anti-emetic – levomopromazine
 NB morphine orally to subcutaneous = 50%
 Opioids – act on CNS on mu, kappa and delta  give medications regularly, by mouth when
possible and using the ladder
o Non-opioid with adjuvant  mild opioid  strong opioid
 Mild opioids – codeine/tramadol
 Strong
o 1st line - Morphine/diamorphine
o 2nd line - Oxycodone/fentanyl transdermal patch
 Opioid naiive – 2.5mg 4 hourly, PRN, change to MR with PRN for breakthrough pain
o Mild to strong – MR morphine BD dose _ immediate release of morphine 1/6 TDD
 SE of opioids include nausea, vomiting, constipation, hiccups, sweating, dry mouth, vivid
dreams, drowsiness, pruritis, hyperalgesia
  Toxicity – myoclonus, pin-point pupils, hallucinations, delirium, sedation, respiratory
depression
o REVERSE with naloxone
Chest X-Ray
 Things to recognize
o Normal
o CHF
o Consolidation
o Effusions
o Masses
o Atelectasis
o Pneumothorax
 NB L only 2 lobes with oblique fissure
 R 3 lobes with oblique fissure and horizontal fissure above
 CHF signs
o Thickening of interlobular septa – Kerley B lines
o Peri-bronchial cuffing – wall hairline thin
o Thickening of fissures – fluid in subpleural space in continuity with interlobular septa
o Pleural effusions
o Enlarged heart – more than ½ thoracic width
 Consolidation
o Air bronchogram – bronchi (air filled), alveoli (fluid)
o Lobar anatomy
o Silhouette sign – no contrast between structures
 Effusions
o Fluid in pleural space
o Meniscus sign
 Masses – cancer/metastases/vascular/TB (ghon focus, calcified LN),
 Pneumothorax – air between visceral and parietal pleura
o Tension – shift of mediastinum, good lung compressed
o Hyperlucency – loss of vascular markings
 Abdominal film interpretation
o Gas pattern – normal, obstruction, ileus
o Calcification
o Soft tissue
o Bones
o Everything else
 Obstruction
o Small bowel – dilated loops, air/fluid levels  adhesions, hernia, intussusception
o Large – distended colon  cancer, volvulus, hernia, inflammation
 Ileus can be localized or generalized
 Calcification
o Urinary stones
o Gall stones
o Vascular – aortic wall, aneurysm, phleboliths
o Masses
 Soft tissue
o Ascites
o Mass effect
o Psoas sign – loss of psoas shadow – appendicitis
 o Hepato/splenomegaly
Type 1 Diabetes – Management DKA
 T1DM – destruction of beta cells on pancreas, genetically susceptible, environmental triggers
o Associated also with autoimmune thyroid disease, coeliac disease and pernicious
anaemia
o Triggers – viral infection, coxsakie, EBV, rubella, mumps, hygiene theory, BSA (cows
milk),
 DKA – life-threatening – lack of insulin, liver produces keto acids for metabolism of AA and
fatty acids, ketone bodies main source of energy – produces two ketoacids (acetoacetic
acid), to form acetone
o ACIDOSIS
 Hyperglycemia, hyperketonaemia, metabolic acidosis,
o Fluid and electrolyte depletion
o Kussmaul respiration – hyperventilation
o Abdominal pain, confusion, coma, dehydration
 Severe when ketones over 6mmol/l, bicarb over 5, pH under 7, hypokalaemia, GCS under 12,
sats under 92%, systolic BP under 90, HR over 100 and under 60 and raise anion gap  ANY
OF THESE then consider HDU admission
 TREATMENT
o Insulin – dose based on weight, sliding scale – fixed rate IV insulin infusion
o Fluids – 0.9% sodium chloride
o Monitor potassium – add 40mmol/l
o ABCDE
Examination of Renal Patient
 Classic renal cases
o PCKD
o CRF
o Renal transplant
 In hospital due to dialysis, will show signs, theme often around renal failure
 Chronic disease history usually (as no PC often)
o Introduction
o Timeline
o PC – lethargy, HTN, blood test, kidney problems as child, family history of kidney
disease
o Progression from diagnosis, when started on dialysis, what types
o Bring to present
o Screen for complications
 NB all symptoms arise from the roles of the kidney failing
o Calcium homeostasis – can’t convert active form of vitamin D (calcitriol) and can’t
resorb calcium, suffer from hypo and hypercalcaemia depending on whether they
are secondary or tertiary hyperparathyroidism
 Hypo – cramps, tingling peripherally
 Hyper – bone pain, constipation, kidney stones
o Blood pressure and fluid homeostasis – accumulates, peripheral and pulmonary
oedema (orthopnea)
o Acid-base balance – control pH, excrete H+ and resorb HCO3- (acidosis with N/V)
o Electrolyte balance – retain Na+ and excrete K+
 Hyperkalaemia – lethargy, muscle paralysis, chest pain
 Hyponatraemia – muscle cramps, N+V, anorexia
 o Erythropoietin – EPO, anaemia common in CKD, lethargy, pallor, SOB, cold
peripheries, chest pain, dizziness
 PMHx – open question, diabetes, HTN and childhood infections
 DHx – NSAID use, operations, transplant, allergies
 Sx – smoking, alcohol, occupation with dialysis
 FHx – PCKD, PCOS, artheriopaths
 ICE – when they first had symptoms did they know, any concerns on current condition, has
care met expectations
 Examination – GI/General
o At end of bed – well/unwell, pale (anaemia), breathing (acidosis compensation),
fistula
o Hands – pallor, perfusion, gouty tophi, fistula, BP, pulse, Lindsay nails???
o Face – pallor, xanthelasma, offer fundoscopy (HTN retinopathy), assess JVP
o Abdomen – inspect, comment on scars (flanks = transplant), palpate, percuss and
auscultate (renal bruits)
 OFFER lung bases
o Ankles for oedema
 For fistula look for signs of infection, aneurysms, wound breakdown, palpate carefully
(should vibrate), and auscultate for bruits to confirm function
 Offer CV exam and neuro exam (PCKD)????
 Other investigations – bedside tests, blood pressure in both arms, lying and standing, ECG
(hyperkalaemia), urine dip (protein and send for albumin creatinine ratio), weight
o Bloods – FBC for anaemia, U&E for urea and creatinine for kidney function, bone for
calcium and phosphate, LFTS (ALP raised in renal bone disease), parathyroid
hormone and VBG/ABG
o Imaging – AXR for renal calculi, USS, CT (stones but use of contrast), MRA (real
vascular disease), biopsy
 Management – many people involved, educate patient on diet and symptoms of
decompensation, control HTN, reduce CV risk (statin/antiplatelets), bone disease
(supplements), anaemia (EPO injections), diabetes control and avoid nephrotoxic drugs
 Acute on chronic presentations
o Hyperkalaemia
o Pulmonary oedema
o AKI
Referral Letter
 Patient details, NHS number, date, where you are
 DIAGNOSIS
 History (relevant +ve/-ve), examination, why they need to come in/be see/why off baseline
 PMH, drugs, social history, DNACPR
 Attached clinical summary
 MEDICAL SCHOOL SAY – interpretation of history, bullet point treatment and PMH, say what
has been done so far, relevant differential diagnosis, requests of
investigations/investigations and results if already done
 Things to include for effective triage – specialty/subspecialty that patient referred to,
referrer details, GP name, practice name, address, phone number, date of referral, patient
details, name, sex, DoB, NHS number, address, telephone number, medical history, current
medication, significant history (previous consultation for condition/name of consultant),
active problems, clinical information, referral priority, reason for referral, preliminary
investigations/management, information regarding social/special circumstances (eg
interpreter, deaf, blind, mobility impairment)
  Be clear and concise, make sure you tailor the letter to who will read it, explain why referral
is needed functionally, describe relevant social issues, use print outs for detailed
history/investigations/highlight important information, tell the specialist what you expect
from them, provide differential diagnoses. Advise on ICE is important, explain if
stress/anxiety to colleague
 Consider who to refer to, the department or a particular consultant
 Simple referral – one or two lines to adequately describe the problems, explain why the
procedure requested is needed, describe social issue
 Print outs from clinical system – ensure any 3rd party information is removed
 If complicated – state in first paragraph if unsure of diagnosis, highlight key points/events in
the history, summarise thoughts
 Do not be afraid to display ignorance and ask for help with the problem
 Emergency referrals – short, highlight key medical, drug and social history
 Referral to other health care workers
 Express yourself clearly – supporting/endorsing a particular action point
o If you do not want to refer you can use phrases such as ‘please see this patient who
requests your opinion on’
GP Pharmacology
 CAP – strep pneumoniae
o Amoxicillin 500mg TDS
o Clarithromycin 500mg BD
o Doxycycline 200mg (BD then OD)  photosensitivity
 NB macrolide + statin = pain
 Doxycycline – photosensitivity
 COPD exacerbation
o AS above – doxycycline, lower threshold
o Haemophilus influenza B
 OM – concerns if over 4 days, discharge, and unwell 6 months, systemically unwell, treat
with antibiotics if bilateral or unilateral and symptom score over 8 with fever, increased
irritability, poor sleep, poor appetite, crying etc
o Amoxicillin (syrup)
o Clarithromycin
o Co-amoxiclav
 Tonsilitis – swab, likely streptococcus, CENTOR/FEVER PAIN SCORING
o Phenoxymethylpenicillin for 10 days (amoxicillin if young)
o Clarithromycin or azithromycin in paeds
 NB amoxicillin EBV rash
 Sinusitis
o Penicillin V
o Clarithromycin
o Doxycycline
 Sacrlet fever – sandpaper rash on trunk, saved in sparing of folds, strawberry tongue, fever,
white coated tongue
o Penicillin V (7 days) or amoxicillin if unable to swallow tablets
o Azithromycin
 Acne
o Benzyl peroxide (red/dry/bleaching)
o Retinoids
o Topical v oral Abx (doxycycline, erythromycin, lymecycline, oxytetracycline)
 Do not take tetracyclines with milk
  Cellulitis (staph aureus)
o Flucloxacillin 500mg QDS (b-lactamase)
o Clarithromycin
 Impetigo – saph
o Fusidic acid topically
o Flucloxacillin 500mg QDS
o Clarithromycin
 Facial cellulitis – co-amoxiclav 625mg
 Bites
o Co-amoxiclav
o Metronidazole and doxycycline (second line/allergy)
 Metronidazole – cannot drink alcohol
 C DIFF DRUGS
o Cephalosporins
o Ciprofloxacin
o Co-amoxiclav
o Clindamycin
 Diverticulitis
o Co-amoxiclav
o Metronidaole (400mg TDS) with ciprofloxacin
 Chlamydia
o Azithromycin 1g STAT (can give in pregnancy and BF)
o Doxycycline 100mg BD 7/7
 Pyelonephritis
o Co-amoxiclav
o Ciprofloxacin BV for 7 days)
 DAMNN DRUGS  AKI
o Diuretic
o ACEI
o Metformin
o NSAIDs
o Nitrofurantoin
 UTI (females)
o Nitrofurantoin 100mg BD 3 days due to resistance
o Pivmecillinam
 UTI (males) 7/7
o Trimethoprim
o Nitrofurantoin
 Pregnant women – same as men 7/7
o Trimethoprim – 1st trimester give folic acid as folate antagonist
Drugs to know about
 Sertraline 50-200mg, can use in pregnancy and BF
 Naproxen – NSAID, give with PPI, 500mg BG, watch eGFR (at 45 use with caution/lower and
at 30 stop), not in pregnancy
 Simvastatin – HMG coA reductase, check LFTs at 1/12, stop in pregnancy/breast feeding, for
high cholesterol, prevention Q-Risk, Gi disturbance, muscle aches, 20-80mg, stop with
macrolides
 Ramipril – ACEI, RAAS, for HTN, lowers BP, dry cough, HF (remodeling), DM (microvascular,
urine ACR, lose protein, protects kidneys), 1.25-10mg
 Chloramphenicol – antibiotic eye drops, conjunctivitis, warm compress, hand hygiene, viral
 o SWAB eyes in newborns due to gonorrhea/chlamydia
 Metformin – GI disturbances, lactic acidosis, DM/PCOS, issues with eGFR
 Cerazette – inhibit ovulation, 12-hour window, start 21 days post-natally, can take if breast
feeding
 Methotrexate – folate antagonist, folic acid (not on same day), 1 weekly, RA, psoriasis, SLE,
crohn’s, scleroderma, vasculitis, abortion
o Shared care agreement monitor LFT’s, U+Es, FBC 3/12
 Donepezil – first line for Alzheimer’s, acetylcholinesterase inhibitor, for mild/early dementia
o NB increase ACh SE – increase frequency, vomiting, anorexia, rash, diarrhea,
agitation, cramps, nausea, insomnia, weight loss
 Warfarin – anti-coagulant, monitor INR, P450, not in pregnancy/BF, reversible with vitamin K
 DOAC – reversal agents, bleeding, well tolerated, no many interactions, issues with renal
function – edoxaban commonly used
 Temazepam – driving/heavy machinery, GABA, sedation, addictive
 Hydrocortisone – steroid cream
 Microgynon – COCP, take 21 days, 7 day break, issues with cover if missed pill in last week or
first week
 Amlodipine – CCB, HTN, HF, 5 + 10 mg, high SE profile, peripheral swelling, rashes, cannot
use in pregnancy/BF
o Nifedipine – used in pregnancy
o OD – metabolic acidosis, nausea, vomiting, coma tx with glucagon
Menstrual Cycle
 Usually lasts 28 days, ovulation 14 days
 Control
o Hypothalamus produces GnRH
o Binds to pituitary stimulating release of LH and FSH
o FSH binds to ovaries stimulating development of ovarian follicles, secretion
oestrogen, secretion of inhibin  development of follicle most sensitive becoming
dominant and Graafian follicle
o LH – binds to ovaries causing production of oestrogen for ovulation and thickening
of endometrium, conversion of Graafian follicle into progesterone producing corpus
luteum and then causing endometrium to become receptive to implantation of
fertilized ovum
o Oestrogen, progesterone and inhibin cause -ve feedback reducing GnRH, LH and FSH
o In pregnancy these remain inhibited causing cessation of menstruation
 Follicular phase – at start of cycle levels of FSH rise causing stimulation of few ovarian
follicles, these mature and compete for dominance, the mature one will produce oestrogen
and inhibits growth of other follicles (this is Graafian follicle), this continues to secrete
oestrogen (which causes endometrial thickening and thinning of cervical mucus to allow
easier passage of sperm), it inhibits LH production, when oestrogen hits a threshold is causes
a spike in LH around day 12 (LH SURGE), the LH causes the membrane of the follicle to
become thin, and this ruptures within 24-48 hours causing release of a secondary oocyte,
this matures into an ootid and then mature ovum that is released into the peritoneal space
and taken into fallopian tube by fimbriae
 Luteal phase – once ovulation has occurred LH and FSH cause the Graafian follicle to develop
into the corpus luteum that produces progesterone (increase in basal body temperature,
endometrium receptive to blastocyst implantation, increased oestrogen production by
adrenals and -ve feedback to stop LH and FSH), as LH and FSH drop corpus luteum
degenerates, therefore no progesterone, causing bleed
 o If ovum fertilized it produced hCG which is similar to LH, preventing the
degeneration of corpus luteum, continuing progesterone, preventing menstruation
(from 8 weeks the placenta overtakes the role of the corpus luteum)
 Uterine cycle
o Functional layer – grows thicker in response to oestrogen and is shed in
menstruation
o Basal layer – foundation layer
 PHASES
 Proliferative – exposure to oestrogen, increasing vascularity, endometrial thickness and
secretory glands
 Secretory phase – ovulation occurred, drive by progesterone, endometrial glands secrete to
allow implantation
 Menstrual phase – end of luteal phase, causing decrease in progesterone, causing spiral
arteries in functional endometrium to contract, the loss causes the functional endometrium
to become ischaemic and necrotic and therefore sheds
 FERTILITY = between 5 days before ovulation until 1-2 days after
Gonadal Axis In Men
 Hypothalamus, pituitary and gonads
 IN MEN
o Hypothalamus releases GnRH
o GnRH to anterior pituitary causing release of LH and FSH
o LH and FSH to testicles
o LH stimulates Leydig cells in testicles to produce testosterone (for spermatogenesis)
o FSH to Sertoli cells to produce androgen binding globulin and inhibin
 ABG bids to testosterone to keep I tin seminiferous tubules
 Inhibin supports spermatogenesis and inhibits FSH, LH and GnRH
o Increasing levels of testosterone and inhibin cause -ve feedback

Vasculitis
 GCA – raised ESR/CRP, temporal arteritis, large vessel vasculitis, first and worst headache in
elderly, visual consequences, scalp tenderness, jaw claudication
 Syphilis – painless non-purulent ulcer, then rash, uveitis, alopecia, fever, rash,
LNadenopathy, then aortitis, iritis, Argyll Robertson pupil, neurological system
 Takayasu aortitis – pulseless disease, systemic vasculitis of large arteries (aorta and brances)
causing MI, TIA, strokes, visual disturbances, claudication,
 Bechet’s – systemic vasculitis of large, medium and small vessels, painful ulcers in mouth,
erythema nodosum, painful genital ulcers, joint involvement, VTE, CNS
 Kawasaki disease – under 5, fever, bilateral conjunctivitis, polymorphous rah, strawberry
tongue, red palms/soles, oedema, skin peeling, cervical LNadenopathy (can lead to coronary
arteritis)
 Wegner’s granulomatosis – granulomatous, multi-organ involvement, mouth ulcers,
epistaxis, rhinitis, otitis media, CN lesions, lung symptoms, HTN, eye signs, long prodrome of
nasal stuffiness, headaches, nose bleeds and hearing difficulties, high c-ANCA
 Churg-Strauss – eosinophilic granulomatosis of lungs, linked to asthma, raised p-ANCA,
affects pulmonary circulation, coronary/cerebral/splanchnic circulations
 MPA – microscopic polyangiitis – necrotizing vasculitis of small vessels, GN and lung, pANCA,
renal, pulmonary, GI, skin, and neurological symptoms
 PAN – polyarteritis nodosa – uncommon, male, middle aged, multi-organ necrotizing
vasculitis, medium sizes vessels, coronary arteritis, HTN, renal failure, GI symptoms, linked to
hepatitis B, mononeuritis multiplex
  HSP – children, purpuric rash over buttocks/extensors, following URTI, urticarial, nephritis,
arthralgia, abdominal pain, self-limiting
Extras
 Appendicitis – erect CXR and AXR
 VTE assessment – gender, age, weight/waist circumference, COCP/HRT, previous diagnosis,
family history, lung disease, IBD, pneumonia, thrombophilia, varicose veins, lower limb
paralysis, immobility (long haul flight, surgery), heart issues, cancer, pregnancy/perinatal (12
weeks), smoking,
 Cord Compression - back pain awake at night, weakness of lungs, incontinent urine and
faeces
 Abdo x-ray
o A – air – pneumoperitoneum, rigler sign, football sign,
o B - bowel
o D – dense structures, calcification, bone – ribs, vertebral column, pelvic bones,
femoral head/neck, calcification in renal/aorta/gallbladder
o O – organ/soft tissue
o X – external objects and artifacts
 Gait patterns
o Hemiplegic gait – unilateral weakness on affected side, arm flexed, adducted and
internally rotated, leg on same side is extended with plantar flexion, drags leg in
circumduction due to foot drop and hypertonia, common in stroke, often mild
hemiparesis, loss of normal arm swing and slight circumduction
o Diplegic gait - both sides with spasticity in lower limbs worse to upper, narrow base,
dragging legs, scraping toes, seen in cerebral palsy (bilateral periventricular lesions),
extreme tightness of hip adductors, scissor gait
o Neuropathic gait – foot drop, lift leg high to not drag foot, unilateral in peroneal
nerve palsy and L5 radiculopathy, bilateral them ALS, DM
o Myopathic – weakness in hip girdle muscles causing drop on contralateral side
(Trendelenburg sign), waddling if bilateral
o Choreiform (hyperkinetic gait), as in basal ganglia disorders (huntington’s), chorea,
dystonia, irregular, jerky, involuntary movements in all extremities
o Ataxic/cerebellar gait – clumsy, staggering with wide based gait, titubation (swagger
back and forth), not be able to walk heel to toe/straight line, truncal instability
o Parkinsonian gait – rigidity and bradykinesia, stooped neck, flexion at knees, little
steps, difficulty initiating steps, involuntary inclination to take acceleration steps
(festination)
o Sensory gait – due to lack of proprioception, slam foot on the floor to feel it,
stomping gait seen in dorsal column issues (B12 deficiency) or peripheral nerves
(DM)